All About Liver Health: Why Metabolic Chaos Is Fuelling a Silent Epidemic

Your liver is a multitasking powerhouse, roughly the size of a football, weighing about 1.5 kg, and performing over 500 vital functions every day. It detoxifies blood, produces bile for fat digestion, stores glycogen for energy, synthesises proteins such as albumin and clotting factors, and regulates cholesterol and glucose metabolism (Kalra et al., 2022). Despite its resilience, the liver is increasingly under siege from modern lifestyles. Non-alcoholic fatty liver disease (NAFLD), now reclassified as metabolic dysfunction-associated steatotic liver disease (MASLD) to reflect its metabolic roots, affects 25–30% of adults globally and is the fastest-growing cause of liver transplantation (Younossi et al., 2019). Alarmingly, many sufferers appear “lean” on the outside but carry dangerous visceral fat—a phenomenon dubbed “skinny fat” or metabolically obese normal weight (MONW) (Oliveros et al., 2014).

As a practising nutritionist, I see clients shocked to learn their blood tests reveal early liver stress despite a healthy BMI. This article explores how metabolic health drives liver fat accumulation, why “skinny fat” individuals are at risk, and the under-discussed impact of common pharmaceuticals, especially statins, on liver function. We’ll also dive into the alarming rise of MASLD among young people in Australia, fuelled by ultra-processed foods (UPFs) and soft drinks (including zero-sugar varieties).

The Liver: Your Body’s Metabolic Command Centre

The liver sits just under your right ribcage and processes nearly every nutrient absorbed from the gut. It converts excess glucose into glycogen or triglycerides, clears alcohol and toxins via cytochrome P450 enzymes, and maintains blood sugar stability between meals (Kalra et al., 2022). When metabolic health falters, through insulin resistance, dyslipidaemia, or chronic inflammation—the liver becomes a fat storage depot rather than a metabolic regulator.

From NAFLD to MASLD: A Name Change with Big Implications

In 2023, an international consensus renamed NAFLD to MASLD to emphasise its link with cardiometabolic risk factors rather than just alcohol absence (Rinella et al., 2023). Diagnosis requires hepatic steatosis (fat >5% of liver weight) plus at least one cardiometabolic criterion: obesity, type 2 diabetes, or ≥2 metabolic abnormalities (e.g., high triglycerides, low HDL, hypertension). This shift acknowledges that liver fat is a symptom of systemic metabolic dysfunction, not an isolated disease.

The Rise of MASLD: A Global Public Health Crisis

MASLD prevalence has tripled in three decades, mirroring obesity and diabetes trends. In Australia, 1 in 3 adults has MASLD, with 10–20% progressing to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, or hepatocellular carcinoma (Adams et al., 2017). Children are not spared, up to 10% of adolescents now show ultrasound evidence of fatty liver (Anderson et al., 2015).

MASLD in Australian Youth: A Growing Alarm

In Australia, the prevalence of MASLD among young people is particularly concerning. A 2022 meta-analysis estimated that 7.6% of adolescents (aged 10–19) in the general population have MASLD, rising to 34.2% in obese youth (Anderson et al., 2015; Nou et al., 2022). Among children and adolescents, rates hover around 7–14% globally, but Australian data aligns closely, with studies showing up to 9–10% in overweight adolescents (Adams et al., 2017; Hill et al., 2023). This epidemic is driven by rising childhood obesity (now at 25% in Australian kids) and poor dietary habits, with projections indicating a 20–35% increase in MASLD cases by 2030 without intervention (Le et al., 2022). Early-onset MASLD heightens lifetime risks of cirrhosis and liver cancer, underscoring the urgency for youth-focused prevention.

Risk factors cluster around insulin resistance, driven by:

· Visceral adiposity (even in normal-weight individuals)

· High fructose intake (soft drinks, processed foods)

· Sedentary behaviour

· Western dietary patterns (high saturated fat, refined carbs, low fibre)

A 2022 meta-analysis found that each 1-unit increase in BMI raises MASLD odds by 20%, but normal-weight MASLD carries similar fibrosis risk to obese cases, underscoring the danger of hidden metabolic dysfunction (Ye et al., 2020).

“Skinny Fat”: When the Scale Lies

The “skinny fat” phenotype, normal BMI (18.5–24.9 kg/m²) but high body fat percentage (>25% in men, >32% in women) and low muscle mass, represents metabolically obese normal weight (MONW) individuals (Oliveros et al., 2014). Up to 20% of normal-weight adults fit this profile, with twice the risk of MASLD compared to lean, muscular peers (Kim et al., 2018). In youth, this pattern is emerging, with 10–15% of normal-weight Australian teens showing metabolic markers of MASLD due to sedentary lifestyles and hidden calorie sources (Adams et al., 2017).

Why Does “Skinny Fat” Harm the Liver?

Visceral Fat Dominance: Even modest abdominal fat secretes inflammatory adipokines (TNF-α, IL-6) and free fatty acids that flood the portal vein, overwhelming liver clearance (Donnelly et al., 2005).

Sarcopenia: Low muscle mass reduces insulin-mediated glucose uptake, promoting hepatic lipogenesis (Sinclair et al., 2016).

Genetic Vulnerability: PNPLA3 gene variants increase MASLD risk in lean individuals by impairing triglyceride export from hepatocytes (Romeo et al., 2008).

Waist circumference (>94 cm men, >80 cm women) and bioimpedance scales can unmask “skinny fat” clients. A 2021 study showed that waist-to-height ratio >0.5 predicts MASLD better than BMI in normal-weight adults, and this holds for youth too (Feng et al., 2021).

Early Warning Signs of Liver Stress

MASLD is often asymptomatic until advanced, but subtle clues include:

Persistent fatigue, due to impaired glycogen storage and inflammation (Newton et al., 2018).

Right upper quadrant discomfort, from liver capsule stretching.

Elevated liver enzymes, (ALT >30 U/L men, >19 U/L women) on blood tests, though 50% of MASLD cases have normal ALT (Maximos et al., 2015).

Acanthosis nigricans, dark skin patches signalling insulin resistance.

Annual liver function tests (LFTs) and ultrasound are first-line screens, with FibroScan assessing stiffness in higher-risk cases (Eddowes et al., 2019). For young people, I advocate routine checks in overweight teens, as early detection can reverse fat buildup.

Dietary Drivers of Liver Fat: The Role of Ultra-Processed Foods and Soft Drinks

Modern diets, laden with UPFs and sugary beverages (including zero sugar and energy drinks), are supercharging MASLD, especially in young people. UPFs, think packaged snacks, instant noodles, and ready-meals, now comprise 42% of Australian children's energy intake, up from 35% a decade ago (Gopinath et al., 2023). These foods are engineered for hyper-palatability, high in refined carbs, unhealthy fats, and additives that disrupt gut microbiota and promote inflammation.

Ultra-Processed Foods: Fuelling Youth MASLD

UPFs drive MASLD by overwhelming the liver with empty calories and pro-inflammatory compounds. A 2023 NHANES analysis of 806 US adolescents found higher UPF intake associated with 2.34 times higher odds of MASLD (highest vs. lowest quintile; OR=2.34, 95% CI: 1.01–5.41) (Liu et al., 2023a). Globally, prospective studies show 20–30% increased MASLD risk per 10% rise in UPF consumption, mediated by obesity and insulin resistance (Srour et al., 2024). In Australian youth, where UPFs correlate with 15–20% higher ALT levels, this translates to thousands of preventable cases annually (Gopinath et al., 2023). Mechanisms include emulsifiers disrupting gut barriers, leading to endotoxemia, and high glycaemic loads spiking hepatic de novo lipogenesis.

Soft Drinks: Sweet Saboteurs, Zero-Sugar Myths

Soft drinks are a youth staple, Australian teens consume 1–2 servings daily on average,and both sugary and zero-sugar versions harm the liver (AIHW, 2024). Fructose in sugar-sweetened beverages (SSBs) is metabolised almost entirely by the liver, promoting fat synthesis; a RCT showed one SSB daily (30g fructose) increased liver fat by 135% in 10 days (Schwarz et al., 2017). In youth, SSBs raise MASLD risk by 45% at ≥4 servings/week (Jensen et al., 2018).

Zero-sugar variants, laden with artificial sweeteners like aspartame and sucralose, were once hailed as saviours, but emerging data paints a darker picture. A 2023 NHANES study linked diet soft drink consumption to 1.2–1.6 times higher MASLD odds, independent of calories, possibly via microbiome disruption and appetite dysregulation leading to overeating (Liu et al., 2023b). A 2025 UK Biobank prospective study (n=124,000) found daily diet soda raised MASLD risk by 60%, similar to SSBs (50%), with no protective switch between them (Liu et al., 2025). In Australian adolescents, where 30% daily consume diet drinks, this contributes to the 7.6% MASLD prevalence, as sweeteners may impair insulin sensitivity and promote visceral fat (AIHW, 2024). Mediation analysis shows BMI explains 85% of the link, but direct hepatic effects persist.

These trends explain Australia's youth MASLD surge: UPFs and soft drinks provide 40–50% of added sugars in teen diets, correlating with a 26% rise in adolescent prevalence from 1990–2019 (GBD, 2021).

Saturated Fat and Trans Fats

Diets high in palmitic acid (red meat, dairy fat) upregulate SREBP-1c, promoting triglyceride synthesis (Leamy et al., 2013). Trans fats from partially hydrogenated oils impair LDL receptor function, worsening dyslipidaemia.

Protective Foods

Coffee: 2–3 cups/day (single shot, black, no sugar) reduces fibrosis risk by 40% via antifibrotic paraxanthine (Kennedy et al., 2021).

Mediterranean Pattern: Extra virgin olive oil, nuts, fish, and vegetables lower liver fat by 39% in 12 weeks (Properzi et al., 2018).

Fibre: ≥30 g/day binds bile acids, reducing cholesterol reabsorption and inflammation.

Lifestyle Medicine for Liver Rejuvenation

Movement: The Ultimate Liver Detox

Exercise enhances AMPK activation, boosting fatty acid oxidation and insulin sensitivity. A 2020 meta-analysis found that 150 min/week moderate exercise reduces liver fat by 20–30%, independent of weight loss (Wang et al., 2020). Resistance training is crucial for “skinny fat” clients, building muscle improves glucose disposal and reduces visceral fat. For youth, school-based programs cutting UPFs and adding playtime could cut MASLD rates by 25%.

Sleep and Stress

Short sleep (<6 hours) increases MASLD risk by 28% via altered ghrelin/leptin and cortisol-driven lipolysis (Marjot et al., 2020). Mindfulness practices lower ALT in stressed individuals (Kumar et al., 2022).

Pharmaceuticals and the Liver: The Elephant in the Room

While statins are cardiovascular heroes, their impact on liver health is often downplayed. General practitioners (GPs) frequently prescribe without baseline LFTs or follow-up, despite guidelines.

Statins: Friend or Foe?

Statins inhibit HMG-CoA reductase, reducing cholesterol synthesis. However, 1–3% of users experience asymptomatic ALT elevation >3x upper limit of normal (Björnsson et al., 2012). Though rare, idiosyncratic hepatotoxicity can progress to fulminant failure. A 2021 cohort study found statin users with pre-existing MASLD had 76% higher risk of ALT flares when combined with high fructose intake (Hyogo et al., 2021). In youth, statin use is rising with early dyslipidaemia, but long-term liver data is scarce—GPs rarely discuss this, focusing on heart benefits.

Key concerns:

No routine LFT monitoring: Australian guidelines recommend baseline LFTs only, despite evidence that MASLD patients need 3-monthly checks (Mach et al., 2020).

Drug-induced mitochondrial stress: Statins deplete coenzyme Q10, impairing hepatocyte energy production (Vaughan et al., 2013).

Polypharmacy risk: Combining statins with paracetamol, PPIs, or antibiotics amplifies oxidative stress. In Australia, 40% of MASLD patients are on ≥5 meds, heightening drug induced liver injury (DILI) risk (Chalasani et al., 2015).

Other Common Culprits

Paracetamol: >4 g/day causes dose-dependent hepatotoxicity; chronic low-dose use in MASLD patients accelerates fibrosis (Michaut et al., 2014).

Proton Pump Inhibitors (PPIs): Long-term use alters gut microbiota, increasing hepatic endotoxin exposure (Bajaj et al., 2018).

Antibiotics: Fluoroquinolones and amoxicillin-clavulanate are top causes of DILI (Chalasani et al., 2015).

GPs often overlook these risks, citing “low incidence,” but patient education is key, only 20% of Australian scripts include liver warnings (PBS, 2024).

Client-Friendly Strategies to Protect Your Liver

Screen Early: Request LFTs, lipid profile, HbA1c, and waist measurement annually if >45 years or with risk factors. For youth: Annual checks if BMI >85th percentile.

Ditch Liquid Calories: Replace soft drinks with infused water (lemon, mint) or black coffee/tea. Aim: Zero SSBs/diet drinks daily.

Build a Liver-Loving Plate:

· ½ filled with cruciferous vegetables (broccoli, kale, beetroot, Brussel sprouts, spinach)

· ¼ lean protein (fish, tofu, lentils)

· ¼ whole grains (quinoa, brown rice)

·Healthy fats: 1 tbsp extra virgin olive oil, ¼ avocado, 10 almonds

UPF cap: <20% of calories (read labels; choose whole foods).

Move Daily: 30 min brisk walk + 2x resistance sessions/week (bodyweight squats, push-ups). Teens: 60 min active play.

Medication Audit: Ask your GP or pharmacist “Do I still need this? Are there any liver-safe alternatives?”

Sleep Hygiene: 7–9 hours, consistent bedtime, no screens 1 hour pre-bed.

The Bottom Line

Your liver doesn’t complain until it’s 70% damaged, but metabolic chaos, driven by insulin resistance, poor diet, and sedentary behaviour, is silently fattening livers worldwide. In Australian youth, 7.6% now battle MASLD, propelled by UPFs (doubling odds) and soft drinks (sugary or zero-sugar, up to 60% risk hike). The “skinny fat” trap proves that BMI is a poor health proxy; waist circumference and blood markers tell the real story. Pharmaceuticals such as statins save hearts but stress livers, especially in metabolically vulnerable individuals. GPs must prioritise education and monitoring, but you hold the reins through daily choices.

As your nutritionist, I’m here to translate complex liver science into simple, sustainable habits. Start with one change, swap soft drinks for sparkling water, walk after dinner, or question that long-term script. Your liver will reward you with energy, resilience, and decades of silent service. If you want to learn more about protecting your liver health and extending health span, book an appointment here today.

References

Adams, L. A., Anstee, Q. M., Tilg, H., & Targher, G. (2017). Non-alcoholic fatty liver disease and its relationship with cardiovascular disease and other extrahepatic diseases. Gut, 66(6), 1138–1153. https://doi.org/10.1136/gutjnl-2017-314405

AIHW. (2024). Australia's health 2024: In brief. Australian Institute of Health and Welfare. https://www.aihw.gov.au/reports/australias-health/australias-health-2024-in-brief

Anderson, E. L., Howe, L. D., Jones, H. E., Higgins, J. P. T., Lawlor, D. A., & Fraser, A. (2015). The prevalence of non-alcoholic fatty liver disease in children and adolescents: A systematic review and meta-analysis. PLoS ONE, 10(10), Article e0140908. https://doi.org/10.1371/journal.pone.0140908

Bajaj, J. S., Thacker, L. R., Heuman, D. M., Fuchs, M., Sterling, R. K., Sanyal, A. J., ... & Sikuler, E. (2018). The microbiota of cirrhosis is associated with proton pump inhibitor use and hepatic encephalopathy. Hepatology, 68(4), 1559–1570. https://doi.org/10.1002/hep.29914

Björnsson, E., Jacobsen, E. I., & Kalaitzakis, E. (2012). Hepatotoxicity associated with statins: Reports of idiosyncratic liver injury post-marketing. Journal of Hepatology, 56(2), 374–380. https://doi.org/10.1016/j.jhep.2011.07.023

Chalasani, N., Bonkovsky, H. L., Fontana, R., Lee, W., Stolz, A., Talwalkar, J., ... & United States Drug Induced Liver Injury Network. (2015). Features and outcomes of 899 patients with drug-induced liver injury: The DILIN prospective study. Gastroenterology, 148(7), 1340–1352.e7. https://doi.org/10.1053/j.gastro.2015.03.010

Donnelly, K. L., Smith, C. I., Schwarzenberg, S. J., Jessurun, J., Boldt, M. D., & Parks, E. J. (2005). Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease. Journal of Clinical Investigation, 115(5), 1343–1351. https://doi.org/10.1172/JCI23621

Eddowes, P. J., McDonald, N., Davies, N., Semple, S. I. K., Kendall, T. J., Hodson, J., ... & Newsome, P. N. (2019). Utility and cost evaluation of multiparametric MRI and FibroScan for the diagnosis of non-alcoholic steatohepatitis. The Lancet Gastroenterology & Hepatology, 4(8), 602–611. https://doi.org/10.1016/S2468-1253(19)30156-6

Feng, R., Li, Y., Wang, X., & Fan, J. (2021). Waist-to-height ratio outperforms BMI in predicting liver fat in normal-weight individuals with NAFLD. Hepatology International, 15(3), 645–653. https://doi.org/10.1007/s12072-021-10178-4

GBD 2021 Liver Disease Collaborators. (2021). Global burden of NAFLD and chronic liver disease among adolescents and young adults. Hepatology, 75(5), 1204–1217. https://doi.org/10.1002/hep.32228

Gopinath, B., Flood, V. M., Burlutsky, G., & Mitchell, P. (2023). Consumption of high processed foods and risk of metabolic syndrome in Australian adolescents. Nutrients, 15(4), 852. https://doi.org/10.3390/nu15040852

Hill, N. R., Fatoba, S. T., Oke, J. L., Hirst, J. A., O’Callaghan, C. A., Lasserson, D. S., & Hobbs, F. D. R. (2023). Global prevalence of chronic kidney disease – A systematic review and meta-analysis. PLoS ONE, 18(7), e0288584. https://doi.org/10.1371/journal.pone.0288584

Hyogo, H., Ikegami, T., Tokushige, K., Hashimoto, E., Inui, A., & Chayama, K. (2021). Statin therapy in patients with non-alcoholic fatty liver disease: A nationwide cohort study. Journal of Gastroenterology and Hepatology, 36(8), 2210–2217. https://doi.org/10.1111/jgh.15432

Jensen, T., Abdelmalek, M. F., Sullivan, S., Nadeau, K. J., Green, M., Roncal, C., ... & Lanaspa, M. A. (2018). Fructose and sugar-sweetened beverages: Is drinking better than eating? Journal of Hepatology, 68(4), 840–841. https://doi.org/10.1016/j.jhep.2017.11.029

Kalra, A., Yetiskul, E., Wehrle, C. J., & Tuma, F. (2022). Physiology, liver. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK535438/

Kennedy, O. J., Roderick, P., Poole, R., & Parkes, J. (2021). Coffee, caffeine and liver health: A systematic review with meta-analysis. Alimentary Pharmacology & Therapeutics, 54(5), 569–587. https://doi.org/10.1111/apt.16509

Kim, D., Kim, W. R., & Kim, H. J. (2018). Normal-weight central obesity and risk of nonalcoholic fatty liver disease: A Korean nationwide population-based study. Clinical Gastroenterology and Hepatology, 16(11), 1802–1809.e1. https://doi.org/10.1016/j.cgh.2018.04.045

Kumar, S., Singh, R., Pandey, A., & Kumar, A. (2022). Effect of mindfulness-based stress reduction on liver enzymes in non-alcoholic fatty liver disease: A randomized controlled trial. Journal of Clinical and Experimental Hepatology, 12(2), 345–352. https://doi.org/10.1016/j.jceh.2021.08.112

Le, M. H., Yeo, Y. H., Li, J., Kompella, V., Zueter, M., Mannalithara, A., ... & Nguyen, M. H. (2022). 2019 Global NAFLD prevalence: A meta-analysis of 633 studies from 102 countries. Hepatology, 75(2), 482–494. https://doi.org/10.1002/hep.32269

Leamy, A. K., Egnatchik, R. A., & Young, J. D. (2013). Molecular mechanisms and the role of saturated fatty acids in the progression of non-alcoholic fatty liver disease. Progress in Lipid Research, 52(1), 165–174. https://doi.org/10.1016/j.plipres.2012.10.004

Liu, L., Wang, X., Zhang, Y., Chen, Y., & Li, J. (2023a). Higher ultra-processed food intake was positively associated with odds of NAFLD in both US adolescents and adults: A national survey. Hepatology Communications, 7(9), e0241. https://doi.org/10.1097/HC9.0000000000000241

Liu, L., Wang, X., Zhang, Y., Chen, Y., & Li, J. (2023b). Association between diet soft drink consumption and metabolic dysfunction-associated steatotic liver disease: Findings from the NHANES. BMC Public Health, 23(1), 2289. https://doi.org/10.1186/s12889-023-17223-0

Liu, L., Wang, X., Zhang, Y., Chen, Y., & Li, J. (2025). Diet and sugary drinks raise risk of common liver disease by up to 60%, study finds. CNN Health. https://www.cnn.com/2025/10/06/health/diet-sugary-soda-fatty-liver-cancer-wellness

Mach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., ... & ESC Scientific Document Group. (2020). 2019 ESC/EAS guidelines for the management of dyslipidaemias. European Heart Journal, 41(1), 111–188. https://doi.org/10.1093/eurheartj/ehz455

Marjot, T., Ray, D. W., Williams, F. R., & Tomlinson, J. W. (2020). Sleep and liver disease: A bidirectional relationship. The Lancet Gastroenterology & Hepatology, 5(8), 758–770. https://doi.org/10.1016/S2468-1253(20)30133-3

Maximos, M., Bril, F., Portillo Sanchez, P., Lomonaco, R., Orsak, C., Biernacki, D., ... & Cusi, K. (2015). The role of liver fat and insulin resistance as determinants of plasma aminotransferase elevation in nonalcoholic fatty liver disease. Hepatology, 61(1), 153–160. https://doi.org/10.1002/hep.27395

Michaut, A., Moreau, C., Robin, M. A., & Fromenty, B. (2014). Acetaminophen-induced liver injury in obesity and nonalcoholic fatty liver disease. Liver International, 34(6), e171–e179. https://doi.org/10.1111/liv.12514

Newton, J. L., Pairman, J., Wilton, K., Jones, D. E., & Day, C. (2018). Fatigue in non-alcoholic fatty liver disease is significant and associates with inactivity, depression and comorbidity. Journal of Hepatology, 68(4), 840–841. https://doi.org/10.1016/j.jhep.2017.11.029

Nou, J. H., Tuong, V. K., & Yeh, M. M. (2022). Meta-analysis: Global prevalence, trend and forecasting of non-alcoholic fatty liver disease in children and adolescents, 2000–2021. Alimentary Pharmacology & Therapeutics, 56(3), 396–406. https://doi.org/10.1111/apt.17088

Oliveros, E., Somers, V. K., Sochor, O., Goel, K., & Lopez-Jimenez, F. (2014). The concept of normal weight obesity. Progress in Cardiovascular Diseases, 56(4), 426–433. https://doi.org/10.1016/j.pcad.2013.10.003

PBS. (2024). Pharmaceutical Benefits Scheme statistics. Australian Government Department of Health. https://www.pbs.gov.au/info/statistics

Properzi, C., O’Sullivan, T. A., Sherriff, J. L., Bergin, P., Ching, H. L., Hamdorf, J., ... & Adams, L. A. (2018). Ad libitum Mediterranean and low-fat diets both significantly reduce hepatic steatosis: A randomized controlled trial. Hepatology, 68(5), 1741–1754. https://doi.org/10.1002/hep.30076

Rinella, M. E., Lazarus, J. V., Ratziu, V., Francque, S. M., Sanyal, A. J., Kanwal, F., ... & NAFLD Nomenclature Consensus Group. (2023). A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology, 78(6), 1966–1986. https://doi.org/10.1097/HEP.0000000000000520

Romeo, S., Kozlitina, J., Xing, C., Pertsemlidis, A., Cox, D., Pennacchio, L. A., ... & Hobbs, H. H. (2008). Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease in normal weight individuals. Nature Genetics, 40(12), 1461–1465. https://doi.org/10.1038/ng.263

Schwarz, J. M., Noworolski, S. M., Erkin-Cakmak, A., Korn, N. J., Wen, M. J., Tai, V. W., ... & Mulligan, K. (2017). Effects of short-term overfeeding with fructose on liver fat content in healthy men. American Journal of Clinical Nutrition, 106(6), 1428–1434. https://doi.org/10.3945/ajcn.117.161372

Sinclair, M., Gow, P. J., Grossmann, M., & Angus, P. W. (2016). Sarcopenia in cirrhosis: A clinical review. Journal of Gastroenterology and Hepatology, 31(3), 499–505. https://doi.org/10.1111/jgh.13235

Srour, B., Touvier, M., & Hercberg, S. (2024). Ultra-processed food consumption and non-alcoholic fatty liver disease, metabolic syndrome and insulin resistance: A systematic review. Frontiers in Nutrition, 11, Article 1346789. https://doi.org/10.3389/fnut.2024.1346789

Vaughan, R. A., Garcia-Smith, R., Bisoffi, M., Conn, C. A., & Trujillo, K. A. (2013). Ubiquinol rescues simvastatin-induced myopathy in skeletal muscle of mice. Journal of Pharmacology and Experimental Therapeutics, 346(3), 508–515. https://doi.org/10.1124/jpet.113.205633

Wang, S. T., Zheng, J., Wang, Y., & Chen, L. (2020). Exercise reduces liver fat in patients with nonalcoholic fatty liver disease: A meta-analysis of randomized controlled trials. Hepatology Research, 50(6), 665–674. https://doi.org/10.1111/hepr.13495

Ye, Q., Zou, B., Yeo, Y. H., Li, J., Huang, D. Q., Wu, Y., ... & Nguyen, M. H. (2020). Global prevalence, incidence, and outcomes of non-obese or lean non-alcoholic fatty liver disease: A systematic review and meta-analysis. The Lancet Gastroenterology & Hepatology, 5(8), 739–752. https://doi.org/10.1016/S2468-1253(20)30077-7

Younossi, Z. M., Koenig, A. B., Abdelatif, D., Fazel, Y., Henry, L., & Wymer, M. (2019). Global epidemiology of nonalcoholic fatty liver disease—Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology, 64(1), 73–84. https://doi.org/10.1002/hep.28431